About: Insulin-Like Growth Factor 1 Regulates Acute Inflammatory Lung Injury Mediated by Influenza Virus Infection

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Insulin-Like Growth Factor 1 Regulates Acute Inflammatory Lung Injury Mediated by Influenza Virus Infection
Creator	Wang, Rong Bai, Miao Dong, Derong Li, Guiping Shi, Yun Zhang, Can Zhang, Chuanfu Zhou, Lijuan Zou, Wei Jones, Ian Mcauley, Julie
Source	Medline; PMC
abstract	The acute inflammatory lung injury is an important cause of death due to influenza A virus (IAV) infection. Insulin-like growth factor 1 (IGF1) played an important role in the regulation of inflammation in the immune system. To investigate the role of IGF1 in IAV-mediated acute inflammatory lung injury, the expression of IGF1 and inflammatory cytokines was tested after IAV A/Puerto Rico/8/1934 (H1N1; abbreviated as PR8) infection in A549 cells. Then, a BALB/c mouse model of PR8 infection was established. On days 3, 5, 7, and 9 post-infection, the mice lung tissue was collected to detect the expression changes in IGF1 mRNA and protein. The mice were divided into four groups: (1) PBS (abbreviation of phosphate buffered saline); (2) PR8 + PBS; (3) PR8 + IGF1; and (4) PR8 + PPP (abbreviation of picropodophyllin, the IGF1 receptor inhibitor). The body weight and survival rate of the mice were monitored daily, and the clinical symptoms of the mice were recorded. On day 5 post-infection, the mice were sacrificed to obtain the serum and lung tissues. The expression of inflammatory cytokines in the serum was detected by enzyme linked immunosorbent assay; lung injury was observed by hematoxylin-eosin staining; the viral proliferation in the lung was detected by real-time quantitative PCR; and the protein expression of the main molecules in the phosphatidylinositol-3-kinases/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase (MAPK) signaling pathways was detected by Western blot. It was found that IGF1 expression is upregulated in A549 cells and BALB/c mice infected with PR8, whereas IGF1 regulated the expression of inflammatory cytokines induced by PR8 infection. Overexpression of IGF1 aggravated the IAV-mediated inflammatory response, whereas the inhibition of IGF1 receptor reduced such inflammatory response. The phosphorylation of IGF1 receptor triggered the PI3K/AKT and MAPK signaling pathways to induce an inflammatory response after IAV infection. Therefore, IGF1 plays an important immune function in IAV-mediated acute inflammatory lung injury. IGF1 may provide a therapeutic target for humans in response to an influenza outbreak, and inhibition of IGF1 or IGF1 receptor may represent a novel approach to influenza treatment.
has issue date	2019-11-26(xsd:dateTime)
bibo:doi	10.3389/fmicb.2019.02541
bibo:pmid	31849847
has license	cc-by
sha1sum (hex)	ae94601843c7f14fc95e723c9bce16232b0bfd70
schema:url	https://doi.org/10.3389/fmicb.2019.02541
resource representing a document's title	Insulin-Like Growth Factor 1 Regulates Acute Inflammatory Lung Injury Mediated by Influenza Virus Infection
has PubMed Central identifier	PMC6887893
has PubMed identifier	31849847
schema:publication	Front Microbiol
resource representing a document's body	covid:ae94601843c7f14fc95e723c9bce16232b0bfd70#body_text
is schema:about of	named entity 'Puerto Rico' named entity 'cells' named entity 'PPP' named entity 'IAV' named entity 'expression' named entity 'influenza A virus' named entity 'regulated' named entity 'immune function' named entity 'IGF1' named entity 'hematoxylin-eosin' named entity 'mouse' named entity 'mice' named entity 'Acute' named entity 'KINASE' named entity 'SERUM' named entity 'COLLECTED' named entity 'KINASES' named entity 'WESTERN BLOT' named entity 'REAL-TIME QUANTITATIVE PCR' named entity 'INHIBITOR' named entity 'CHANGES' named entity 'SURVIVAL RATE' named entity 'BALB' named entity 'PLAYS' named entity 'PBS' named entity 'UPREGULATED' named entity 'IGF1' named entity 'LUNG TISSUE' named entity 'PI3K' named entity 'ACUTE' named entity 'SIGNALING PATHWAYS' named entity 'DAILY' named entity 'INHIBITION' named entity 'RECORDED' named entity 'REGULATION' named entity 'PICROPODOPHYLLIN' named entity 'ROLE' named entity 'MEDIATED' named entity 'MOUSE MODEL' named entity 'DAY 5' named entity 'EOSIN' named entity 'PR8' named entity 'STAINING' named entity 'IMMUNE FUNCTION' named entity '2F8' named entity 'MAPK SIGNALING' named entity 'PHOSPHATE BUFFERED SALINE' named entity 'OBTAIN' named entity 'FOUND' named entity 'MODEL OF' named entity 'HEMATOXYLIN' named entity 'GROUPS' named entity 'OVEREXPRESSION' named entity 'INDUCED' named entity 'DIVIDED' named entity 'POST' named entity 'ENZYME LINKED IMMUNOSORBENT ASSAY' named entity 'LUNG' named entity 'IGF1 RECEPTOR' named entity 'RICO' named entity 'REDUCED' named entity 'MONITORED' named entity 'PLAYED' named entity 'OBSERVED' named entity 'TO DETECT' named entity 'MICE' named entity 'PHOSPHATIDYLINOSITOL' named entity 'CLINICAL SYMPTOMS' named entity 'INSULIN-LIKE GROWTH FACTOR 1' named entity 'INFLAMMATORY' named entity 'INFLAMMATION'

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